• Title of article

    Analyses of methylation status of CpG islands in promoters of miR-9 genes family in human gastric adenocarcinoma

  • Author/Authors

    -، - نويسنده Department of Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran Ebrahimi-Askari, Raziyeh , -، - نويسنده Department of Genetics, School of Biological Sciences, Tarbiat Modares University, Tehran, Iran Behmanesh, Mehrdad , -، - نويسنده Department of Hematology, Faculty of Medicine, Tarbiat Modares University, Tehran, Iran Soleimani, Masoud

  • Issue Information
    فصلنامه با شماره پیاپی 0 سال 2015
  • Pages
    10
  • From page
    73
  • To page
    82
  • Abstract
    -
  • Abstract
    In the recent years deregulation for microRNAs expression pattern have emerged as a possible molecular factor for carcinogenesis. It has been reported that the expression of miR-9 was down-regulated in human gastric adenocarcinoma. To figure out the molecular mechanism of this down regulation, the methylation status in promoters of miR-9 family loci were compared in the human gastric adenocarcinoma samples with their normal margins. Using a methylation specific PCR technique the methylation status of miR-9 family loci were compared between 30 pairs of primary human gastric adenocarcinoma samples with their normal margins. The methylation of miR 9-1 status showed no specific difference in promoter methylation pattern in tumor and normal specimens, while in the miR-9-2 locus were unmethylated in both types of tissues. The promoter of miR-9-3 locus seems to be specifically methylated in tumor and their normal margin tissues. Our data revealed methylation of these CpG islands were not meaningfully different between normal and tumor gastric adenocarcinoma specimens and the methylation status of promoter may not be able to account for alteration of miR-9 expression in this type of gastric cancer.
  • Journal title
    Molecular Biology Research Communications
  • Serial Year
    2015
  • Journal title
    Molecular Biology Research Communications
  • Record number

    2136359